Blog Archive

Monday, 28 January 2008

Weekly BioNews 21 - 28 Jan 2008

- Scientists create gene map for synthetic life

Fri Jan 25, 2008 4:22am ESTBy Maggie Fox, Health and Science Editor

WASHINGTON (Reuters) - Researchers have assembled the entire genome of a living organism -- a bacterium -- in what they hope is an important step to creating artificial life. The bug, Mycoplasma genitalium, has the smallest known genome of any truly living organism, with 485 working genes. Viruses are smaller, but they are not considered completely alive as they cannot replicate by themselves. Bacteria can and do, and the team at the non-profit J. Craig Venter Institute in Maryland has been working for years to try to build M. genitalium from scratch."We consider this the second in significant steps of a three-step process in our attempts to make the first synthetic organism," Craig Venter, founder of the institute, told a telephone briefing."This entire process started with four bottles of chemicals." M. genitalium has a fairly simple structure -- all its DNA is carried on a single chromosome. Chromosomes are the structures that carry genetic material, and the entire code is called the genome. Other genetic material called RNA is needed to convert this gene map into something a cell can use to function.

Publication Represents Largest Chemically Defined Structure Synthesized in the Lab

Team Completes Second Step in Three Step Process to Create Synthetic Organism

ROCKVILLE, MD—January 24, 2008—A team of 17 researchers at the J. Craig Venter Institute (JCVI) has created the largest man-made DNA structure by synthesizing and assembling the 582,970 base pair genome of a bacterium, Mycoplasma genitalium JCVI-1.0. This work, published online today in the journal Science by Dan Gibson, Ph.D., et al, is the second of three key steps toward the team’s goal of creating a fully synthetic organism. In the next step, which is ongoing at the JCVI, the team will attempt to create a living bacterial cell based entirely on the synthetically made genome.

The team achieved this technical feat by chemically making DNA fragments in the lab and developing new methods for the assembly and reproduction of the DNA segments. After several years of work perfecting chemical assembly, the team found they could use homologous recombination (a process that cells use to repair damage to their chromosomes) in the yeast Saccharomyces cerevisiae to rapidly build the entire bacterial chromosome from large subassemblies.

“This extraordinary accomplishment is a technological marvel that was only made possible because of the unique and accomplished JCVI team,” said J. Craig Venter, Ph.D., President and Founder of JCVI. “Ham Smith, Clyde Hutchison, Dan Gibson, Gwyn Benders, and the others on this team dedicated the last several years to designing and perfecting new methods and techniques that we believe will become widely used to advance the field of synthetic genomics.”

(Jan. 25, 2008) — The British-American biotech company Acambis reports the successful conclusion of Phase I trials of the universal flu vaccine in humans. The universal influenza vaccine has been pioneered by researchers from VIB and Ghent University. This vaccine is intended to provide protection against all ‘A’ strains of the virus that causes human influenza, including pandemic strains. Therefore, this vaccine will not need to be renewed annually. Influenza (flu) is an acute infection of the bronchial tubes and is caused by the influenza virus. Flu is highly contagious and causes people to feel severely ill. An average of 5% of the world's population is annually infected with this virus. In Belgium, an average of 1500 people die of flu each year. A "more severe flu year" − such as the winter of 1989-1990 − claimed in Belgium alone, 4500 victims. Moreover, occasionally pandemics occur.

This negative-stained transmission electron micrograph (TEM) depicts the ultrastructural details of an influenza virus particle, or "virion". A member of the taxonomic family Orthomyxoviridae, the influenza virus is a single-stranded RNA organism. (Credit: Cynthia Goldsmith)

The use of a drug to activate stem cells that differentiate into bone appears to cause regeneration of bone tissue and be may be a potential treatment strategy for osteoporosis, according to a report in the February 2008 Journal of Clinical Investigation. The study – led by researchers from Massachusetts General Hospital (MGH) and the Harvard Stem Cell Institute (HSCI) – found that treatment with a medication used to treat bone marrow cancer improved bone density in a mouse model of osteoporosis, apparently through its effect on the mesenchymal stem cells (MSCs) that differentiate into several types of tissues.

“Stem cell therapies are often thought of as putting new cells into the body, but this study suggests that medications can turn on existing stem cells that reside in the body’s tissues, acting as regenerative medicines to enhance the body’s own repair mechanisms,” says David Scadden, MD, director of the MGH Center for Regenerative Medicine and HSCI co-director. “Drugs that direct immature cells to become a particular cell type, like in this study, could potentially be very useful.”

The study was designed to examine whether the drug bortezamib (Bzb), which can alleviate bone destruction associated with the cancer multiple myeloma, could also regenerate bone damaged by non-cancerous conditions. In their first experiments, the researchers showed that treating mice with Bzb increased several factors associated with bone formation. Similar results were seen when cultured MSCs were treated with Bzb, but not when the drug was applied to cells that were committed to become particular cell types. Found in the bone marrow, MSCs have the potential to develop into the bone-building osteoblasts and several other types of cells – including cartilage, fat, skin and muscle.

- Search for the 'on' switches may reveal genetic role in development and disease

January 25, 2008 06:02 PM

“The majority of DNA in our bodies is packaged, or tightly structured,” said Gregory Crawford, Ph.D., a researcher in the IGSP and one of the senior investigators on this study. “Our goal was to identify the areas of DNA across the entire genome that are not packaged, because we know those are the regions that are important in regulating gene activity.”

The researchers published their findings in the January 25, 2008 issue of the journal Cell. The study was funded by the Duke IGSP and the National Human Genome Research Institute. They combined two known processes to look at regulatory regions across the whole human genome, Crawford said.

“We used an enzyme called DNase that has been known for decades to preferentially identify unpackaged regions of DNA,” he said. “In this study, we identified all unpackaged regions within the entire genome using two extremely efficient methodologies: microarrays and sequencing.”

Just as many scientists had given up the search, researchers have discovered that the pancreas does indeed harbor stem cells with the capacity to generate new insulin-producing beta cells. If the finding made in adult mice holds for humans, the newfound progenitor cells will represent “an obvious target for therapeutic regeneration of beta cells in diabetes,” the researchers report in the Jan. 25 issue of Cell, a publication of Cell Press.

“One of the most interesting characteristics of these [adult] progenitor cells is that they are almost indistinguishable from embryonic progenitors,” said Harry Heimberg of the JDRF Center at Vrije Universiteit Brussel in Belgium and the Beta Cell Biology Consortium. “In terms of their structure and gene expression, there are no major differences. They look and behave just like embryonic beta cell progenitors."

Insulin is required for cells to take up blood sugar, the body’s primary energy source. In people with certain types of diabetes, blood sugar rises due to an inability of pancreatic beta cells to produce insulin in sufficient quantities.

Genes have the ability to recognise similarities in each other from a distance, without any proteins or other biological molecules aiding the process, according to new research published this week in the Journal of Physical Chemistry B. This discovery could explain how similar genes find each other and group together in order to perform key processes involved in the evolution of species.

This new study shows that genes – which are parts of double-stranded DNA with a double-helix structure containing a pattern of chemical bases - can recognise other genes with a similar pattern of chemical bases.

This ability to seek each other out could be the key to how genes identify one another and align with each other in order to begin the process of ‘homologous recombination’ – whereby two double-helix DNA molecules come together, break open, swap a section of genetic information, and then close themselves up again.

Recombination is an important process which plays a key role in evolution and natural selection, and is also central to the body’s ability to repair damaged DNA. Before now, scientists have not known exactly how suitable pairs of genes find each other in order for this process to begin.